Hydrologic refugia, plants, and climate change.

Climate, physical landscapes, and biota interact to generate heterogeneous hydrologic conditions in space and over time, which are reflected in spatial patterns of species distributions. As these species distributions respond to rapid climate change, microrefugia may support local species persistence in the face of deteriorating climatic suitability. Recent focus on temperature as a determinant of microrefugia insufficiently accounts for the importance of hydrologic processes and changing water availability with changing climate. Where water scarcity is a major limitation now or under future climates, hydrologic microrefugia are likely to prove essential for species persistence, particularly for sessile species and plants. Zones of high relative water availability - mesic microenvironments - are generated by a wide array of hydrologic processes, and may be loosely coupled to climatic processes and therefore buffered from climate change. Here, we review the mechanisms that generate mesic microenvironments and their likely robustness in the face of climate change. We argue that mesic microenvironments will act as species-specific refugia only if the nature and space/time variability in water availability are compatible with the ecological requirements of a target species. We illustrate this argument with case studies drawn from California oak woodland ecosystems. We posit that identification of hydrologic refugia could form a cornerstone of climate-cognizant conservation strategies, but that this would require improved understanding of climate change effects on key hydrologic processes, including frequently cryptic processes such as groundwater flow

HYPOXIC PULMONARY VASOCONSTRICTION

It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution